The 76 amino acid recombinant protein has a predicted molecular mass of approximately 8,685 Da. The DTT-reduced protein migrates at approximately 8kDa and non-reduced protein migrates at approximately 13kDa by SDS-PAGE. The N-terminal amino acid is Glycine.

10-100µg sizes are bottled at 200µg/mL. 500µg sizes and larger are bottled at the concentration indicated on the vial.

Storage & Handling:

Unopened vial can be stored between 2°C and 8°C for one month, at -20°C for six months, or at -70°C for one year. For maximum results, quick spin vial prior to opening. The protein can be aliquoted and stored from -20°C to -70°C. Stock solutions can also be prepared at 50-100 µg/mL in sterile buffer (PBS, HPBS, DPBS, or EBSS) containing carrier protein such as 0.2-1% BSA or HSA and stored in working aliquots at -20°C to -70°C. Avoid repeated freeze/thaw cycles.

CCL2, also known as MCP-1, is a member of the CC ß chemokine family. It is widely expressed in endothelial cells, smooth muscle cells and monocytes in response to several atherogenic stimulants such as CD40 ligand, platelet derived growth factor (PDGF), interleukin-1β (IL-1β) and oxidized low density lipoprotein. Several recent in vivo studies have disclosed critical roles of MCP1 in atherosclerosis. In addition, MCP-1 has been implicated in monocytic infiltration of tissues during several inflammatory diseases, and has been implicated in macrophage-mediated tumor growth suppression in mice. CCL2 has been shown to have direct effects on tumor cells in an autocrine and paracrine fashion in multiple cancers, including breast, lung, cervix, ovary, sarcoma, and prostate. In addition, MCP-1 plays a key role in the regulation of MMPs during transmigration.MCP-1/CCl2 has been described as a new diagnostic marker and therapeutic target for progressive renal injury in diabetic nephropathy. Kidney epithelial cells, including glomerular podocytes and tubular cells make MCP-1 in response to high glucose and advanced glycation end products. MCP-1 promotes inflammation and progressive injury in diabetic kidneys. The importance of MCP-1 in the early development of diabetic nephropathy has been determined in animal models incorporating genetically deficient mice or therapeutic blockade of MCP-1 receptor (CCR2).

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